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CARDIAC TAMPONADE AND
PERICARDIAL DISORDERS IN
CONNECTIVE TISSUE DISEASES:
CASE REPORT AND LITERATURE
REVIEW
Ricky L. Langley, MD, MPH, and Edward L. Treadwell, MD
Greenville, North Carolina
Pericardial disorders occurring in connective
tissue diseases are not uncommon and may
present as acute or chronic pericarditis with or
without an effusion. In many instances, a
diagnosis of pericardial involvement is not
found until autopsy. Echocardiography and
other currently employed radiographic techniques have enhanced the ability to make a
diagnosis. Approximate frequencies of common connective tissue disorders with pericardial involvement include scleroderma (59%),
systemic lupus erythematosus (44%), mixed
connective tissue disease (30%), rheumatoid
arthritis (24%), and polymyositis/dermatomyositis (11%). Cardiac tamponade or constriction is rare. This article describes a patient
with clinical features consistent with mixed
connective tissue disease that presented with a
pericardial effusion and cardiac tamponade. In
addition, a review of pericardial involvement in
connective tissue diseases and the occurrence
of cardiac tamponade or constriction is included. (J Nati Med Assoc. 1994;86:149-153.)
From the Sections of General Internal Medicine and Rheumatology/Immunology, Department of Medicine, East Carolina
University School of Medicine, Greenville, North Carolina.
Supported by grants from the Arthritis Foundation and American Medical Association-Education and Research Foundation. Requests for reprints should be addressed to Dr Edward L.
Treadwell, Dept of Medicine, Section of Rheumatology/
Immunology, East Carolina University School of Medicine,
Greenville, NC 27858-4354.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 86, NO. 2
Key words * pericardial disorders * mixed connective
tissue disease * cardiac tamponade
Pericardial disorders in connective tissue diseases
such as systemic lupus erythematosus (SLE) may
present as acute or constrictive pericarditis with or
without effusions.' Symptoms may be insidious or may
present suddenly and progress rapidly to acute lifethreatening occurrences. Etiologically, pericardial disorders may be classified as infectious pericarditis,
idiopathic pericarditis (at times, probably due to
undiagnosed viral disease), and pericardial involvement
related to hypersensitivity or autoimmunity.2
Pericardial disorders are not unusual in connective
tissue diseases. However, cardiac tamponade is rare. This
report describes a case of cardiac tamponade in an
individual with clinical features consistent with mixed
connective tissue disease and no previous history of
rheumatologic or cardiac disease. A review of pericardial
disorders in other connective tissue diseases also is
presented.
CASE REPORT
A 26-year-old black male was in good health until 2
weeks before admission when he presented to the
emergency room complaining of chest pain related to
breathing, sore throat, and greenish-yellow sputum.
Physical examination was positive for pharyngitis. Chest
radiograph revealed a small pleural effusion at the left
lower base. Throat, blood, and sputum cultures were
negative. He was treated with a 10-day course of oral
ampicillin, 500 mg three times daily. Three days later, he
returned with complaints of a swollen, tender right elbow
149
CARDIAC TAMPONADE & PERICARDIAL DISORDERS
and a 2-day history of fever and chills. Physical
examination revealed: blood pressure 110/70 mm Hg,
pulse 108 beats/min, respiratory rate 22 breaths/min, and
a temperature of 38.3°C. Breath sounds were decreased in
the region of the left lower lobe with dullness to
percussion and E to A changes. A resting tachycardia was
present without murmurs, gallops, or rubs. The right
elbow was tender, swollen, and warm to touch. He was
admitted for further evaluation.
Admission laboratory studies showed a white blood
cell count (WBC) of 11.1 K/mm3 with a differential of
72% polymorphonuclear cells, 1 1% bands, 5% lymphocytes, 1 % mononuclear cells, 1% eosinophil, and 1%
basophil; a red blood cell count (RBC) of 5.07
million/mm3 with normal indices, and a normal
chemistry profile except for an albumin of 3.1 g/dL
(normal 3.5-5.0) and lactate dehydrogenase 301 IU/L
(normal 100-225). A urinalysis revealed 4 + albumin,
3-5 WBCs per high-power field, 0-2 RBCs per
high-power field, and a few bacteria. A urine culture
was negative. A 24-hour urine test revealed a creatinine
clearance of 83 mL/min (normal 85-125) and a total
protein of 9.3 g/24 hours (normal 25-150 mg/24 hrs).
Fifteen milliliters of purulent fluid was aspirated from
the elbow. An analysis of the fluid demonstrated a WBC
of 38 K/mm3 with 98% polymorphonuclear cells and 2%
mononuclear cells; 6 K/mm3 RBCs; a total protein of 5.1
g/dL (normal 1-3); and glucose of 86 mg/dL (normal
70-110). Gram stains, bacterial cultures, acid-fast bacteria, fungal smears and cultures, and countercurrent
immunoelectrophoresis all were negative. Thoracentesis
of the left lower lobe revealed a WBC of 41.5 K/mm3
with 99% polymorphonuclear cells and 1 % mononuclear
cells (normal WBC < 1000 K/mm3 and <25% polymorphonuclear); total protein of 4.5 g/dL; glucose 52 mg/dL;
pH of 7.14; and lactate dehydrogenase of 714 1U/L. Gram
stains, fungal and acid-fast bacterial smears, countercurrent immunoelectrophoresis, and cultures all were negative. Suspecting an empyema, a chest tube was placed
into the left hemithorax. The patient was treated with a
7-day course of intravenous cefamandole and gentamicin
until cultures were confirmed to be negative.
On the fourth hospital day, a pericardial rub was
noted, and a moderate posterior pericardial effusion was
demonstrated by a two-dimensional echocardiogram.
The patient was noted to have a right-sided pleural
effusion, and a thoracentesis revealed a WBC of 3.6
K/mm3 with 83% polymorphonuclear cells and 17%
mononuclear cells, RBC of 60 K/mm3, total protein of
4.6 g/dL, glucose of 92 mg/dL, lactate dehydrogenase
1240 IU/L, and pH of 7.31. Cultures remained negative.
150
Three days later a repeat echo showed an increased
amount of pericardial fluid but no sign of tamponade.
The next morning he became tachypneic and hypotensive (90/60 mm Hg). His radial pulse was noted to be
50-60 beats/min. A pulsus paradoxus of 12 mm Hg was
noted using a sphygmomanometer. An electrocardiogram demonstrated low voltage and diffuse ST segment
evaluation. He was transferred to the intensive care unit
where an attempted pericardiocentesis was unsuccessful. His condition continued to deteriorate, and a
pericardiostomy was performed and yielded approximately 600 mL of serosanguinous fluid. A Jackson Pratt
drain was placed within the pericardial space. A gram
stain of the pericardial fluid showed few WBCs but was
negative for organisms. Routine bacterial, acid-fast
bacterial, and fungal cultures were negative. A biopsy
of the pericardium showed fibrinous pericarditis with
neutrophilic and lymphocytic infiltrates throughout but
no granulomas. On June 11, 1984, the patient experienced a brief episode of second and third degree heart
block, which required no specific therapy. He remained
asymptomatic from further episodes of heart block and
was transferred out of the intensive care unit.
An antinuclear antibody screen by standard indirect
immunofluorescence3 demonstrated a speckled pattern
with a titer of 1:40 000. An extractable nuclear antigen
was positive for antinuclear ribonucleoprotein (antinRNP) antibodies by double immunodiffusion.3 Antibodies to native deoxyribonucleic acid (nDNA) by the
Crithidia luciliae method, Smith antigen, SS-A(Ro) and
SS-B(Ha,La) by double immunodiffusion3 were negative. A rheumatoid factor and lupus erythematosus prep
were negative. Complements consisting of C3, C4, and
properdin factor B all were within normal limits. An
erythrocyte sedimentation rate was elevated at 72
mm/hr (normal range 0 to 15 mmlhr).
A rheumatologic consultation was obtained and
noted the presence of bilateral knee and ankle effusions,
sclerodactyly, and a history consistent with Raynaud's
phenomenon. In view of the patient's positive antinuclear antibody, anti-nRNP antibody, and other clinical
and laboratory findings, a diagnosis of mixed connective tissue disease was proposed.
The patient was started on prednisone, 1 mg/kg/day
in three divided doses with marked improvement in his
cardiopulmonary symptoms. Eight days later a computerized tomography (CT) scan was performed of his
chest to exclude other possible causes of the pericardial
effusion. No lesions were found, and only a trace
amount of pericardial fluid was noted. His pleural
effusions had completely resolved. A 24-hour urine test
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 86, NO. 2
CARDIAC TAMPONADE & PERICARDIAL DISORDERS
obtained before his discharge showed a decrease in total
protein to 2 g/24h. The patient was discharged on a slow
tapering course of prednisone.
One month later, a repeat CT scan of the chest and
echocardiogram showed complete resolution of the
pericardial effusion and no other pulmonary lesions.
DISCUSSION
Mixed connective tissue disease has been described
as a rheumatic disease syndrome characterized by
features that resemble SLE, rheumatoid arthritis, progressive systemic sclerosis (scleroderma), and
polymyositis/dermatomyositis, with high titers of circulating antibodies against nRNP.4
Since the first description of 25 people with mixed
connective tissue disease,4 the disease entity has been
described extensively, including cases with cardiac
involvement. A clinical evaluation of 16 patients with
mixed connective tissue disease, by Oetgen et al,5
reported a 38% incidence of cardiac abnormalities
including pericarditis, asymmetric septal hypertrophy,
and left ventricular dilatation. In a study by Alpert et a16
of 38 patients with the disease, symptoms potentially
attributed to the cardiovascular system were noted in 32
patients. Cardiovascular examination revealed abnormalities in 30 of 38 patients. Such abnormalities
included acute pericarditis with or without pericardial
effusion, mitral valve prolapse, intimal hyperplasia of
the coronary arteries, perivascular and myocardial
lymphocytic infiltrates including clinical myocarditis,
and pulmonary hypertension.
Cardiac involvement in children with mixed connective tissue disease also was found not to be unusual. In
one study, an evaluation of 14 children with the disease
revealed six with pericarditis and nine with aortic
insufficiency.7
Pericarditis has been the most frequent cardiac
finding in mixed connective tissue disease.8 In a study
by Oetgen et al,5 25% had evidence of pericarditis.
Alpert et al6 noted 29% with pericardial abnormalities
detected by clinical and laboratory findings. A 43%
incidence of pericarditis was detected by Singsen et al.7
Leung et a19 reported 4 of 17 (24%) patients with
pericardial abnormalities by echocardiography. Two
(12%) of these patients had small pericardial effusions.
Nunoda et all described a 55-year-old female with
mixed connective tissue disease who developed perimyocarditis and pericardial effusion. Pericardiocentesis
was performed, and 300 mL of straw-yellow colored
fluid was removed.
The pathogenesis of pericarditis in mixed connective
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 86, NO. 2
TABLE. FREQUENCY OF PERICARDIAL
INVOLVEMENT IN VARIOUS CONNECTIVE
TISSUE DISORDERS
Disorders
%
30.3
Mixed connective tissue disease5-7,9
44
Systemic lupus erythematosusl'12-17
24
Rheumatoid arthritis18-21
58.6
Scleroderma22-26
11.4
Polymyositis/dermatomyositis27-32
*Percentage represents average of referenced studies.
tissue disease is unclear, but Negoro et alII suggest it is
attributable to the activation of the complement system
by locally formed ribonucleic protein immune complexes. Although there is a high frequency of pericardial
involvement in mixed connective tissue diseases, the
incidence of cardiac tamponade is very rare. In a review
of the English literature, only two other cases in
addition to the current case have been reported. In a
study by Alpert et al,6 postmortem examination of four
patients with mixed connective tissue disease was
performed. Pericardial abnormalities were noted in
three out of four patients. A large quantity of
serosanguinous pericardial fluid and diffuse inflammation of the epipericardial surface were noted during
pathologic examination of the patient with cardiac
tamponade. There were widespread fibrin deposition
and infiltration with polymorphonuclear leukocytes on
histologic examination of this case. In another report,9
a patient with a 6-year history of mixed connective
tissue disease had purulent pericarditis and cardiac
tamponade caused by Nocardia asteroides. However,
no information was given detailing other symptoms of
the disease at the time of her tamponade or when the
diagnosis was made in relationship to the event.
The incidence of pericardial involvement has been
found to be high in SLE,1,12-17 rheumatoid arthritis,18121
and scleroderma,22-26 but not in dermatomyositis/
polymyositis.27-32 Pericardial abnormalities were noted
to be much more frequent when using echocardiography or at autopsy compared to clinical evaluation
alone.6,15,18,19,22'33'34 However, the occurrence of tamponade was rare in all these diseases. The table
represents averages of clinical, echocardiographical,
and pathological studies of pericardial disorders in
various connective tissue diseases.
There have been a few reports of tamponade
presenting as the initial manifestation of SLE.12-14,16,17
Studies of patients with SLE have reported a 20% to
50% incidence of clinical pericarditis.12 Pericardial
151
CARDIAC TAMPONADE & PERICARDIAL DISORDERS
fluid ranged in color from serous to hemorrhagic.
Pericardial effusions were detected in 50% by echocardiography, and up to 80% had pericardial involvement
at autopsy.'3'15 Askari et al'2 reviewed several reports
on pericarditis and tamponade in SLE. Of 1116 cases of
SLE, pericarditis was found in 321 (28.7%) and
tamponade in five (0.45%). In the individual series
reviewed, the incidence of tamponade ranged from 0%
to 2%. In a report by Swaak et al,35 a weak association
was found between the presence of anti-nRNP antibodies and pleuropericarditis.
In necropsy studies on patients with rheumatoid
arthritis, the incidence of pericarditis varied from 11% to
50%.18 In a study by MacDonald et al,19 16 of 51 patients
(31%) had echocardiographic evidence of pericardial
effusion. Two other patients were noted to have pericardial thickening. Bacon and Gibson20 found echocardiographic evidence of pericardial effusion in 50%, 15%,
and 0% of patients with chronic nodular rheumatoid
arthritis, typical non-nodular rheumatoid arthritis, and
osteoarthritis, respectively. In a review of the literature on
cardiac tamponade and constrictive pericarditis in rheumatoid arthritis, pericardial tamponade has been documented in association with it in 20 cases18; at the time of
the tamponade, 84% of the patients had moderate to
severe rheumatoid arthritis. Escalant et a12' noted the
prevalence of cardiac compression with tamponade in
rheumatoid arthritis varied from 0.22% to 0.5%.
McWhorter and Leroy22 reviewed records of 210
patients with scleroderma and identified two patterns of
pericardial disorders in 15 patients. One pattern of
chronic pericardial effusion in 11 of 15 patients
occurred in association with chest pain, dyspnea,
cardiomegaly, and symptoms of congestive heart
failure. Another pattern found in four patients consisted
of acute pericarditis with fever, pericardial friction rub,
dyspnea, and chest pain. Early evidence of tamponade
was reported in three patients, but no emergency
intervention was required. Autopsies were performed
on 34 of the 210 patients. Pericardial involvement
(defined as fibrinous or fibrin adhesions or pericardial
effusion of 50 cc or greater) was found in 19 patients
(56%). Sackner et a123 noted pathology of the pericardium as a common feature in 18 of 25 (72%)
postmortem examinations of patients with scleroderma.
D'Angelo et a124 compared 58 autopsied patients with
scleroderma with 58 matched controls and found
pericardial lesions in 55% compared with only 12% of
the controls. However, the incidence of pericardial
effusion was the same as in controls.
There has been an increasing number of reports of
152
cardiac involvement in polymyositis and dermatomyositis.27-32 However, the incidence of pericardial involvement appears small, which may be due in part to
underutilization of echocardiography in evaluation of
patients with these disorders. In a study by Bitnum et
al,30 2 of 13 children had a friction rub and one had a
history of pericardial effusion. Askari and Huettner27
reported two cases of pericardial effusion out of eight
patients evaluated with cardiac abnormalities. In a study
of 21 patients with polymyositis, Gottdiener et al3'
detected 16 (76%) with evidence of cardiac abnormalities, but pericardial effusion was detected in only one
case. In another study,28 67 of 134 (50%) patients were
found to have an abnormal cardiac finding, but no
evidence of pericardial involvement was detected. No
cases of tamponade were reported in the above studies
of patients with polymyositis or dermatomyositis.
The treatment of pericarditis included the use of
nonsteroidal anti-inflammatory drugs with or without
corticosteroids, or removal of the pericardial fluid if
cardiac tamponade existed.6'1215-17,21,22,36,37 Occasionally, resection of the pericardium was required when
constriction of the pericardium was present.18 In most
cases, acute pericarditis was self-limiting and treatment
was primarily symptomatic, using nonsteroidal antiinflammatory drugs to relieve the pain. In instances of
effusion without tamponade, corticosteroids were usually effective in resolving symptoms and eliminating
pericardial fluid. The treatment of cardiac tamponade
was to remove the pericardial fluid and lower pericardial pressure toward normal. This was usually done by
pericardiocentesis or a surgical procedure.
CONCLUSION
Pericardial disorders can occur in various connective
tissue diseases and may be fatal rarely. Pericardial
effusions commonly go undetected clinically in connective tissue diseases and are not found until autopsy. If
pericardial effusion is suspected upon evaluation of a
patient, an echocardiogram should be performed and
followed serially to determine if the effusion is
progressive and to monitor response of the effusion to
therapy. One should be prepared to treat cardiac
tamponade if a patient deteriorates suddenly.
Acknowledgments
The authors thank Dr William Reeves from the Section of
Cardiology for his review and comments and Mrs Debbie
Nichols for preparation of the manuscript.
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